The Drosophilaovarian tumorGene Is Required for the Organization of Actin Filaments during Multiple Stages in Oogenesis

Abstract

The ovarian tumor gene is required during both early and late stages of oogenesis. Mutations produce a range of phenotypes, including agametic ovarioles, tumorous egg chambers, and late stage oogenic arrest. We demonstrate that each of these phenotypes is associated with specific aberrations in actin distribution. In the earliest case, ovarian tumor mutations cause actin filaments to accumulate ectopically in the fusome. This correlates with abnormal fusome morphology and arrested germ cell development in the germaria. Similarly, ovarian tumor function is required for the localization of actin that is essential for the maturation of ring canals. This defect gives rise to tumorous egg chambers in which germ cell numbers and morphology are profoundly aberrant. We also confirm that ovarian tumor is required for the formation of the nurse cell cytoplasmic actin array that is essential for the nonspecific transport of cytoplasmic contents to the oocyte during late oogenesis. Our data suggest that at this stage ovarian tumor controls the site where actin filaments initiate. Taken together, these studies suggest that the diverse ovarian tumor mutant phenotypes derive from the mislocalization of actin filaments, indicating a role for this gene in organizing the female germline cytoskeleton, and that the misregulation of actin can have profound effects on germ cell division and differentiation.

Filopodia-like Actin Cables Position Nuclei in Association with Perinuclear Actin in Drosophila Nurse Cells

“…During dumping, perinuclear actin was also visible with Lifeact-GFP or Fascin-GFP, in the presence of actin cables (Figures 7D and S1A). The presence of perinuclear actin filaments is further supported by two genetic manipulations that stabilized perinuclear actin and increased the perinuclear accumulation of Msp-300 and Cheerio: the expression of the actin-binding domain of Shot (Figures 7F, S5A, and S5B) and mutation of the ovarian tumor gene (Figures S5C–S5E) (Rodesch et al., 1997). …”

Intimate relationships with their neighbors: Tales of stem cells in Drosophila reproductive systems

“…Orb and Sxl, which both can bind mRNAs to regulate their translation or stability, are expressed in GSCs, cystoblasts, and developing cysts (Bopp et al, 1993; Christerson and McKearin, 1994; Lantz et al, 1994). otu encodes two protein isoforms that regulate accumulation of Sxl in germ cells (Bopp et al, 1993; Rodesch et al, 1997). It is likely that these differentiation genes are involved in regulating the stability or translation of mRNAs encoding proteins that are important for cystoblast differentiation.…”

DNA replication in nurse cell polytene chromosomes of Drosophila melanogaster otu mutants

“…It must be emphasized that our analysis did not use wild-type NCs, as these cells lack polytene chromosomes, but rather NCs from otu mutants. This mutation results in disrupted organization of actin filaments and cytoskeleton in NCs (Rodesch et al 1997), which may lead to aberrant cell division and abnormal formation of egg chamber. Three main classes of otu alleles are recognized.…”